Abstract
B7-H4 has an inhibitory effect on immune responses via the down-regulation of T cell-mediated immunity, but how the engagement of B7-H4 molecules by counter molecules affects the signaling mechanism of the B7-H4-expressing cells is poorly defined. In this study, we found that B7-H4 expression was enhanced on B cells infected with Epstein-Barr virus (EBV) and that triggering of these molecules induced apoptosis of EBV-transformed B cells. Engagement of B7-H4 initially increased intracellular level of ROS, which then induced the expression of FasL. Engagement of B7-H4 subsequently provoked Fas-mediated and caspase-dependent apoptosis in association with cytochrome c and AIF, and EndoG was released from the mitochondria on EBV-transformed B cells. These results suggest that B7-H4 may be a potential therapeutic target for EBV involved malignancy diseases.
Original language | English |
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Pages (from-to) | 227-237 |
Number of pages | 11 |
Journal | Cancer letters |
Volume | 266 |
Issue number | 2 |
DOIs | |
Publication status | Published - 2008 Aug 8 |
Externally published | Yes |
Keywords
- Apoptosis
- B cell
- B7-H4
- EBV
- Fas
- FasL
ASJC Scopus subject areas
- Oncology
- Cancer Research